Hypertensive response to stress: The role of histaminergic H1 and H2 receptors in the medial amygdala

- Cimetidine and mepyramine inhibited hypertensive response to stress.
- Central H1 and H2 histaminergic receptors and hypertensive response to stress
- Medial amygdala H1 and H2 histaminergic receptors and hypertensive response to stress

Different brain areas seem to be involved in the cardiovascular responses to stress. The medial amygdala (MeA) has been shown to participate in cardiovascular control, and acute stress activates the MeA to a greater extent than any of the other amygdaloid structures. It has been demonstrated that the brain histaminergic system may be involved in behavioral, autonomic and neuroendocrine responses to stressful situations. The aim of the present study was to investigate the role of the histaminergic receptors H1 and H2 in cardiovascular responses to acute restraint stress. Wistar rats (280-320 g) received bilateral injections of cimetidine, mepyramine or saline into the MeA and were submitted to 45 min of restraint stress. Mepyramine microinjections at doses of 200, 100 and 50 nmol promoted a dose-dependent blockade of the hypertensive response induced by the restraint stress. Cimetidine (200 and 100 nmol) promoted a partial blockade of the hypertensive response to stress only at the highest dose administered. Neither drugs altered the typical stress-evoked tachycardiac responses. Furthermore, mepyramine and cimetidine were unable to modify the mean arterial pressure or heart rate of freely moving rats under basal conditions (non-stressed rats). The data suggest that in the MeA the histaminergic H1 receptors appear to be more important than H2 receptors in the hypertensive response to stress. Furthermore, there appears to be no histaminergic tonus in the MeA controlling blood pressure during non-stress conditions.